Isopropyl Alcohol Ingestion Presenting as Pseudorenal Failure Due to Acetone Interference

Mahathi R. Adla, MD; Julio A. Gonzalez-Paoli, MD; Stephen I. Rifkin, MD, FACP, FASN

Disclosures

South Med J. 2009;102(8):867-869. 

In This Article

Discussion

IPA represents 0.6% of all exposures and 0.3% of all deaths due to poisoning. The estimated minimum lethal dose for adults is approximately 100 mL, but patients have survived ingestions of over 1000 mL.[2] IPA reaches a peak serum level 15-30 minutes after ingestion, with an elimination half-life of 3-7 hours. Ketosis occurs as IPA is metabolized by alcohol dehydrogenase primarily to acetone. Given the higher affinity of alcohol dehydrogenase for ethanol, coingestion of ethanol can block metabolism of IPA and slow its elimination. Serum acetone levels can be detected in blood 15-30 minutes post ingestion and in the urine 3 hours after. Acetone levels rise at a rate comparable to the decline in serum IPA levels and can be persistent in urine for more than 24 hours, even with ingestion of subtoxic quantities.[4]

IPA toxicity is primarily due to the parent compound, manifesting with central nervous system depression similar to ethyl alcohol and myocardial depression with resulting hypotension and shock.[1,5] A high level of IPA will produce an osmolar gap, but acidosis is rare since neither IPA nor acetones are organic acids.[2] Acetone is uncharged, hence the anion gap is normal. Acidosis can occur due to lactic acidosis from hypotension but, otherwise, severe acidosis with IPA ingestion should mandate a search for other coingestants.[3] Acute renal failure is rare with IPA, but can occur secondary to rhabdomyolysis or acute tubular necrosis due to hypotension.[5]

IPA ingestion can present as "pseudo" renal failure due to a spurious elevation of serum creatinine.[5,6] This is attributed to acetone interference with the colorimetric assay for creatinine.[7,8] This will give a false impression of acute renal failure, as it did in our patient who had an extensive work up during multiple admissions to determine the etiology of his renal failure. One of the clues to diagnosis is an isolated serum creatinine elevation with a normal BUN. Most auto analyzer systems use the Jaffe-alkaline-picrate reaction. However, there are many substances which react with picric acid, thus leading to an apparent increase in the serum creatinine concentration. Interfering substances include glucose, acetoacetate, acetone, unconjugated bilirubin, cefoxitin, cefaclor, sulfasalazine, pyruvic acid, ascorbic acid, and nitromethane.[9,10] Most interfering substances cause only minor elevations in the serum creatinine level. However, acetoacetate causes substantial interference with the assay, with levels of about 500 mg/dL overestimating the serum creatinine by 3.5 mg/dL (as measured by UniCel® DxC 800 Synchron® Clinical System, Beckman Coulter Inc, Fullerton, CA). In addition, acetone levels greater than 40 mg/dL can also spuriously overestimate serum creatinine level.[5] Hawley and Falko[5] demonstrated a parallel decline in serum creatinine levels with the fall in serum acetone levels.

When an arterial sample from our patient was tested using a blood gas analyzer (Stat Profile® Critical Care Xpress analyzer, Nova Biomedical, Waltham, MA), a normal serum creatinine concentration was found. An enzymatic assay is used in the determination of creatinine in the blood gas analyzer, thus avoiding the interferences affecting the colorimetric method.[11] The results are obtained in 30 seconds to 2 minutes and offer the fastest method to confirm suspicions of a falsely elevated creatinine. All blood gas machines will do the enzymatic analysis for serum creatinine as long as the appropriate module is added to the machine. In hospitals where enzymatic assay for serum creatinine is a send-out test, it takes about 2-3 days for the results.

The management of IPA depends on the time of ingestion and hemodynamic status of the patient.[2] Since the parent compound is responsible for most symptoms and is rapidly metabolized, most patients do well with conservative management. In hemodynamically unstable patients or with significant respiratory depression or with serum IPA levels greater than 400 mg/dL, hemodialysis is indicated.[1,2] Since acetone is less toxic than IPA, there is no indication for alcohol dehydrogenase inhibition with fomepizole or ethanol.

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